1
Q
Acute respiratory failure definitions
A
Hypoxic (PAO2 <8 kPa OA
Hypercapnic (PaCO2 > 6.7 kPa OA
2
Q
Causes of respiratory failure
A
- Hypoventilation
- respiratory centre depression (drug, anaesthetic, head injury, encephalopathy, fatigue
- Nerve damage (MND, spinal injury, Guillain-Barre
- Neuro muscular junction (paralytic agents, MG)
- Muscle dysfunction (myopathy, fatigue, malnutrition, dystrophy)
- Chest deformities (kyphoscoliosis, ankylosing spondylitis, pleural fibrosis
- Airway obstruction - VP mismatch
- Pneumonia, pulmonary oedema, pulmonary haemorrhage & contusion, intracardiac anatomical shunting - Diffusion abnormality (fibrotic disease, pulmonary oedema, ARDS
3
Q
Causes of breatlessness(in time)
A
Minutes –> Pneumothorax, PE, pulmonary oedema
Hours –> Asthma, pneumonia, pulmonary oedema, metabolic acidosis
Days/more –> Pleural effusion, IECOPD, pneumonia
4
Q
Correlation between oximetry and PaO2
A
100% –> 13.3
90% –> 8
50% –> 3.5
5
Q
Sizing oropharyngeal airways:
A
- Large adult (100mm - guedel 5)
- Medium adult (90mm- guedel 4)
- Small adult (80mm guedel 3)
6
Q
Contraindications to LMA / iGEL
A
- Inability to open mount
- Pharyngeal pathology
- Airway obstruction at / below larynx
- Low pulmonary compliance or high airway resistance
7
Q
Complications of LMA / iLMA
A
Aspiration, gastric insufflation, partial airway obstruction, cough, laryngospasm, post extubation stridor
8
Q
Volume pre-set assist control ventilation
A
Operator set tidal volume and minimum ventilatory rate
Patient & ventilator are able to initiate breaths themselves
Breath characteristics same irregardless of who initiates
9
Q
Pressure pre-set assist control ventilation (pressure control ventilation)
A
Inspiratory pressure is set (not tidal volume
10
Q
Normal tidal volume
A
6-8 ml/kg predicted body weight
11
Q
PEEP starting:
A
5 cmH20 - higher levels usually required in patients with acute pulmonary oedema or ARDS
PEEP = 0 in asthma / COAD who are not taking spontaneous breaths
12
Q
Improving oxygenation + Adverse effects + Range of “safe values”
A
- Increase FiO2 (oxygen toxicity, 0.21-0.5)
- PEEP (note + intrathoracic pressures - CVS & barotrauma; 0-10)
- Increase inspiratory time (gas trapping, +IT pressure; <50% respiratory cycle
- Tital volume / inspiratory pressure (barotrauma; TV <8ml/kg; insp pressure <30 cmH20
- Inspiratory pause (decrease inspiratory flow time (5-10% respiratory cycle time
Minute ventilation should be titrated against pH
13
Q
Causes of high airway pressure / low tidal volumes
A
- Ventilator (settings, malfunction)
- Circuit (kinking, pooling of condensed water vapour, wet filters causing increased resistance
- ETT (kinked, obstruction with sputum/blood, endobronchial intubation)
- Patient (bronchospasm, decreased compliance - oedema, consolidation, collapse, decreased pleural compliance - pneumothorax, decreased chest wall compliance (abdominal distension)
14
Q
How to measure alveolar pressure?
A
Inspiratory pause hold - in apnoeic patients
- Airway pressure = flow x resistance + alveolar pressure
- If flow = 0
- Then airway pressure = alveolar pressure
Activate inspiratory pause hold on ventilator and note airway pressure when plateaus
Alveolar pressure, not airway pressure causes barotrauma / haemodynamic compromise. If possible keep alveolar pressure <30cmH20
15
Q
DDx hypotension after PPV initiation
A
- Hypovolaemia exacerbated by reduced venous return due to rising ITP
- Drugs - almost all anaesthetic induction agents cause vasolidation + myocardial depression
- Gas trapping due to over-enthusiastic ventilation
1a. Give fluids, if doesn’t work disconnect ventilation for 10-30s to release gas
ALWAYS consider tension pneumothorax
16
Q
DDx desaturation on ventilation
A
- Set Fi02 to 1
- Is chest moving
- Yes –> consider endobronchial intubation, pneumothorax, collapse, pulmonary oedema, bronchospasm
- No –> Manually ventilate
- If manual ventilation easy?
- Yes (ventilator problem)
- No (ETT / pt problem)
17
Q
Principles of ventilation: ARDS
A
Heterogenous involvement of lung with areas of consolidation/collapse + relative normal areas
= If normal tidal volume used most of this goes to normal areas = barotrauma
Principle: re-open alveoli + keep them open
- High PEEP + low tidal volume
Tidal volumes 6-8 ml/kg predicted + plateu pressure <30mmH20
- Adjust according to required FIO2
Ventilate in prone position
18
Q
Principles of ventilation: Asthma
A
High resistance, high risk of gas trapping. Alveolar compliance normal
- Maximise expiratory time, short inspiratory time with higher inspiratory flow
- Alveolar pressures unaffected
19
Q
Indications for NIV
A
Respiratory acidosis (pH <7.32)
Hypercapnia (PaCO2 >8 kPa)
Hypoxia (PaO2 <8 kPa despite high FiO2)
20
Q
Contraindications to NIV
A
Severe acidosis (pH<7.1) Inability to protect and maintain airway Coma Agitation Excessive secretions Haemodynamic instability Pneumothorax Oro-facial abnormalities / recent surgery Recent upper GI surgery Apnoea
21
Q
NIV appropriate initial settings:
A
- Inspiratory pressure 8-10 cm H20
- Expiratory pressure 4-6 cm H20
- Backup ventilation rate 12
- Fi02 1.0
- If no improvement in 1-2 hours innovative mechanical ventilation
22
Q
Target urine output:
A
0.5-1 ml/kg/hour in absence of diuretics, dopamine,
23
Q
Changes in CVP with fluid boluses:
A
Measure before & 5 minutes after fluid bolus
0-3 mmHg difference 0 underfilled
3-5 mmHg difference = euvolaemia
>5 mmHg difference = overload
24
Q
Dopamine
A
Short acting, ionotropic, chronotropic, vasoconstrictor effects
In sepsis increases cardiac output with minimal effects on TPR
Greater risk of arrythmias than NA
5ug/kg/min
25
Noradrenaline
Vasoconstrictor with minor direct ionotropic and chronotropic effects
Can increase CO indirectly through increasing diastolic pressure and coronary perfusion
0.05ug/kg/min
26
Epinephrine
Greater chronotropic and ionotropic effects than NA, less vasoconstriction than NA
In immediately life threatening shock epinephrine repeated 0.1mg boluses until severe hypotension reversed
27
Dobutamine
Ionotropic vasodilator and chronotropic effects
Not in hypotensive pts unless combined with NA
0-20 ug/kg/min
28
Shocking values
Biphasic defibrillators - 150-200J in arrest
| Monopolar defib - 360J
29
When do we give three shocks in a row?
1. Non-automated defib available
2. Witnessed onset of arrest
3. Patient already being monitored
4. Cariac surgery immediate post-op
30
Amiodarone dosing cardiac arrest
300 mg/10 minutes
60mg/h 6 hour
30mh/h
Total 2g / day
31
5hs
Hypovolaemia
Hypothermia
H kalaemia
Hypoxia
32
5Ts
```
Tamponade
Tension
Thromboembolism
Trauma
Toxins
```
33
Shocking values arrythmias
Paroxysmal SVT 50-100J
Atrial flutter 50-100
Atrial fibrillation 200
Wide complex tachy 100-200 (100-150 biphasic0
Polymorphic VT (350J monophasic 150-360 biphasic) - not synchronised
34
Polymorphic VT DDx
Polymorphic VT in the context of prolonged QTc = torsades de pointes
Polymorphic VT in context of normal QTc = ischaemic
35
Vaugh-Williams anti arrythmics
1. Na channel (procainamide, lidocaine, flecainide)
2. B blockers
3. Potassium efllux (amiodarone, sotalol
4. Calcium channel (verapamil diltiazem)
5. Unkown/other (adenosine, dioxie
36
Management of torsades
Withdraw precipitant
IV Mg 5-10 mmol / 15 minutes
Isoproterenol
37
Management of bradycardia
Atropine 0.5mg-1mg every 3-5minutes to maximum of 3mg
Isoprenaline infusion 0.5-10microgram (caution IHD)
Pacing for symptomatic bradycardia
38
Indications for urgent transcutaneous pacing
```
Asystole
Symptomatic unresponsive to therapy
Mobitz type II 2nd degree HB
3rd degree HB
Trifascicular block
```
39
When can bicarbonate be effective in hyperkalaemia?
In the presence of acidosis as he Na/H anti port is only active in intracellular acidosis
Useful temporising measure, however most patients with ARF and metabolic acidosis require RRT
40
Nebulised B2 agonists in hyperkalaemia
20-40% patients do not respond
41
Urinary alkalinisation
Prevents re-absorption across renal tubular epithelium = promoted excretion
1-2mmo/kg sodium bicarb IV bolus
Infusion 150 mmol in 1000 ml 5% dex 250 ml / hour
Serum bicarb & k regular
Regular urine dip aim pH >7.5
42
Management of rhabdomyolysis
Aggressive fluid resus, alkalynisation of urine (pH>6.5), maintain polyuria >100ml/h
Identify and treat causative factor (compartment syndrome, status epileptics, heatstroke
43
Rough fluid maintenance values
Water 30ml/kg/day
Na 2 mmol/kg/day
K 1 mmol/kg/day
44
Approximate insensible fluid losses
Faeces - 100ml/day
Lungs - 400ml/day
Skin - 600ml/day
45
Platelet transfusion thresholds in sepsis
Active bleed - 100
<5 all patients
5-10 if additional risks of bleeding
46
Steroids in sepsis
Controversial
May be considered in septic shock when hypotension is poorly responsive
to fluids and vasopressors
Hydrocort 200-300mg/day >5days + tapering
47
Blood Loss vs clinical features
<15% - pulse + bp + RR + CRT NAD, anxious,
15-30% - borderline tachy, BP >100, RR 16-20, CRT+, agitated
30-40% - >110bpm, BP<90, RR 21-26, CRT+, confused
>40%- >120bpm, hypotension+, RR<10/>26, lethargy
48
Needle thoracostomy
Wide bore IV cannula into 2nd IC space mic clavicular line
Syringe with saline
Bubbles when aspirated
49
Principle of massive transfusion in trauma
RBC : PLT : FFP
1:1:1
Tranexamic acid 1g IV stat + 1g IV over 8 hours
50
Mechanisms of RTI + associated injuries
Frontal: C-spine, anterior flail chest, myocardial contuions, pneumothorax, transection of aorta, ruptured liver/spleen, fracture/dislocation hip / knee
Side: C-spine, lateral flail chest, pneumothorax, ruptured spleen.liver, pelvis/acetabular fracture
Rear: C-spine
Vehicle to Pedestrian: Head to toe
51
Trauma injuries: Tension pneumothorax
Resp distress/shock/absence breath sounds+hyperresonance
Needle thoracostomy
Chest drain insertion
52
Trauma injuries: Open Pneumothorax
"Sucking chest wound"
If opening >2/3 diameter of trachea = air will preferentially enter through chest
3 side dressing: flutter-type valve effet
Chest drain
53
Trauma injuries: Tamponade
Penetrating > blunt
Usual signs may be absent
FAST scan +ve - pericardiocentesis
Emergency thoracotomy/sternotomy
54
Trauma injuries: Massive haemothorax
>1500 ml bloods
| Chest drain + emergency thoracotomy
55
Trauma injuries: Traumatic aortic rupture
If survives to hospital = contained rupture
| Cardiothoracics - aortic stenting
56
Trauma injuries: Myocardial contusion
Echo + ECG
| Supportive management
57
Trauma injuries: C spine
Can only be excluded on basis of CT cervical spine + sagittal reconstruction
58
Cerebral perfusion pressure
MAP-ICP
| Monro-Kellie hypothesis - sum of volumes of brain csf and IC blood are constant
59
Cushing's Triad
Bradycardia
Hypertension
Low respiratory rate
60
Principles of managing ICP
Non specific: Nurse at 30% (improve venous drainage), paralysis + sedation (reduce oxygen demand, prevent cough - raise ICP) + analgesia, normothermia (prevent rise in cerebral metabolism) + normal glucose levels (neurological injury)
1. Surgical evacuation / excision
2. Osmotherapy - mannitol (0.25-1g/kg /5min + 0.25-0.5 g/kg 6 hourly) or hypertonic saline (150ml 3% solution). Never prior to haematoma evacuation unless signs of herniation
3. Hyperventilation - only if herniation imminent as will recede brain perfusion. Aim PaCo2 4-4.5 kPa
61
Principles of managing SAH
Prevention of secondary injury, re-bleeding and vasospasm
Maintain cerebral perfusion press >60 with BP <150
Labetalol infusion
Nimodipine if aneurysm suspected in absence of hypotension
62
Principles of management: Status Epilepticus
1. glucose, bloods, O2, left lateral position
* ** In adults with hypoglycaemia give thiamine 100mg first then 50% 50ml IV
2. Either: Diazepam 0.2mg/kg (less preferable) OR Lorazepam 0.1mg/kg IV at 2mg/min or Midazolam 10mg IM if no access
3. Phenytoin 15-20 mg/kg (should be given if diazepam) - <50mg/min (monitor ECG and BP - if hypotension or arrhythmia slow infusion
63
Principles of management: Refractory Status Epilepticus
I&V
Infusion of: thiopentone (3-5mg/kg at 3.5mg/kg/h); proposal 2mg/kg 30-100 ug/kg/min; midazolam (less preferable - tachyphylaxis) at 0.2mg/kg at 0.2 mg/kg/h
64
Assessing the PaO2 in context
P:F ratio --> PaO2/FiO2; Normal 60, PF trio of <25 implies severe reps failure. Not need on air
65
Bohr effect
Haemoglobin's oxygen binding affinity is inversely related to acidity and concentration of Co2
= In areas of active respiration lower binding affinity increases O2 release from Hb
66
Causes of shift of oxygen disassociation curve
```
Right shift (lower affinity) - low pH, high PaCO2, pyrexia, higher 2,3 DPG
Left shift (higher affinity) - high pH, low PaCo2, hypothermia, low 2,3 DPG, congenital haemoglobinopathies
```
67
Anion gap
Na + K - Cl - HCO3 (classic)
However as K levels usually low is is common to omit it
Na-Cl-HCO3
Normal 8-16
Note about 11 mmol of the normal gap = albumin
50% reduction in albumin concentrations reduces anion gap about 6
68
Anion gap and metabolic acidosis
1. Increased (lactate, ketoacidosis - diabetes and alcoholic, salicylates, methanol, ethylene glycol, renal failure - late stage)
2. Normal (GI bicarb loss - diarrhoea, pancreas, biliary, urinary diversion; renal bicarb loss (RTA, ketoacidosis during therapy, renal hypoperfusion)
69
Lactic acidosis - type I & II
I - tissue hypoxia (shock, hypoxaemia, anaemai, post convulsion, sepsis)
II - drugs/disease (metformin, ethanol, methanol, salicylates, paracetamol, DM, RF, leukaemia/lymphoma, pancreatitis, short bowel, thiamine deficiency
70
How often can you get respiratory compensation for metabolic acidosis?
Completes resp compensation for primary metabolic acidosis does not occur
Levels <2.7 kPa are rarely maintained in chronic acidosis
71
Causes of metabolic alkylosis
Volume (chloride depletion) - vomiting, diuretics, post-hypercapnic
Hyperadrenocorticoidism - cushing's, conns, indogenous,
72
Causes of respiratory alkylosis
Hypoxia - acute (pneumonia, asthma, oedema), chronic (IPF, CCHD, altitude, anaemia)
Non hypoxic resp centre stimulation - anxiety, salicylate, cerebral disease, cirrhosis, pregnancy, excessive ventilation
Clinically can cause tetany, confusion, syncope (cerebral vasospasm)
73
Met acid + Resp alkyl
Salicylate
Sepsis
Hepatorenal insufficiency
Coming off a huge etoh binge
74
Met acid + Resp Acid
Post arrest, oedema, sepsis
75
Met alk + reps acid
Chronic resp acidosis pts a metabolic alkylosis superimposed - diuretics, steroids, ventilation. Will reduce acidaemic stimulus to breathe
76
RASS
Richmond agitation sedation score
+4: Combative (immediate danger to staff)
+3: Very agitated (aggressive to staff, pulls tubes & catheter
+2: Agitated (non-purposeful movement, patient-vent dysynchrony)
+1: Restless (anxious/apprehensive)
0: Alert and calm
-1: Drowsy (sustained awakening + eye contact to voice)
-2: Light sedation (brief awakening on voice)
-3: Moderate sedation (movement to voice)
-4: Deep sedation (movement to physical stimulation)
-5: Unrousable
77
Sedation in an un-intubated patient with hypoxia & agitation
Haloperidol 1-2mg IV (caution QT prolongation)
| Midazolam 1mg IV (close monitoring of resp status)
78
Sedation: Propofol
Anxiolysis + hypnosis, reduced reps drive, v. short acting (easily titratable), limited accumulation, not reliant on renal or hepatic excretions, no tolerance, no withdrawal effects
Vasodilation, high lipid load of infusion, anaphylaxis, no analgesic effect
79
Sedation: Morphine & midazolam
Anxiolysis, hypnosis, analgesia, reduced reps drive, better haemodynamic stability
Reliant of renal/hepatic excretion, accumulation, tolerance, withdrawal, delirium, constipation
80
Induction: Propofol
1-1.5mg/kg (>55yr, debilitated, critically ill). Note vasodilation and hypotension potential
81
Paralytics: Suxamethonium
Short acting depolarising neuromuscular blocking agent
1mg/kg
SE: bradycardia, K release, apnoea, malignant hyperthermia
Avoid in sites where K is high or may climb rapidly
82
Paralytics: Rocuronium
Non-depolarising agent
0.9 mg/kg emergency
Infusion 0.5mg/kg/hr
Accumulation, prolonged use causes atrophy, risk of awareness
83
Daily basal energy calculation
kcal/day = 25xBW(kg)
x1. 1 (for each degree C above normal)
x1. 2 (mild/mod stress)
x1. 4 (mod/sev stress)
Miscellaneous FY2
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